We have shown over-expression of NGEP increases cell: cell adhesion and are examining its role in ion transport in collaboration with Dr. Criss Hartzell at Emory. Using a genomic approach in collaboration with Dr. Y. we have shown NGEP is a member of a large family of transmembrane channel like proteins that are activated by calcium. We have shown that the POTE family of genes is pro-apoptotic and work through the BAK pathway to kill target cells. We have generated new monoclonal antibodies to CAPC. Using these specific antibodies we found CAPC resides in the endoplasmic resiculum. Over expression of CAPC causes changes in cell motility and cell growth. We have previously shown mice with partial inactivation of both alleles of ankRD26 are morbidly obese and also larger than normal. The obesity is due to hyperphogia. We have performed two hybrid analyses to identify proteins interacting with ankrd26 and identified two proteins now under study. We are making transgenic mice expressing the normal ankrd26 gene in the brain to determine if it will correct the obesity and hyprphoges. We have examined the mutant mice as a function of age and have found old mice develop liver cancer and plan to study why this occurs. We have prepared fibroblasts from embryos of mutant mice and find they are more readily induced to make adipocytes.